miR-497-5p induces apoptosis in K562 cells by downregulating ROCK1.

OBJECTIVE: To validate the role of miR-497-5p in apoptosis in K562 cells by targeting Rho-associated kinase isoform 1 (ROCK1). METHODS: From January, 2017 to February, 2019, 57 patients with chronic myeloid leukemia (CML) treated in our hospital were included in patient group, and 50 healthy individuals were recruited as control group. miR-497-5p level in peripheral blood was quantitated using qRT-PCR. After transfecting with miR-497-5p overexpression vector and ROCK1 inhibitor, K562 cells were monitored in terms of proliferation (CCK8 assay), migration and invasion (Transwell), and apoptosis (flow cytometry). Binding loci between miR-497-5p and ROCK1 were predicted, and the targeting relationship was confirmed (dual-luciferase reporter (DLR) assay). RESULTS: miR-497-5p was poorly expressed in CML (P < 0.05). Forced overexpression of miR-497-5p or inhibition of ROCK1 suppressed malignant processes (proliferation, proliferation, migration and invasion) in K562 cells and induced apoptosis (P < 0.05). DLR assay revealed a decreased luciferase activity after miR-497-5p binding to ROCK1 (P < 0.05). CONCLUSION: miR-497-5p induces apoptosis in K562 cells by downregulating ROCK1.

miR-506 in patients with chronic myeloid leukemia and its effect on apoptosis of K562 cells.

OBJECTIVE: To explore the expression of miR-506 in chronic myeloid leukemia (CML) and its influence on the biological function of CML cells. METHODS: Altogether 84 CML patients from February 2012 to September 2014 were obtained as the observation group (OG), and 71 healthy people were taken as the control group (CG). miR-506 was tested using RT-qPCR, and the 5-year survival of patients with high and low expression of miR-506 was compared with the median value of miR-506 as the limit. ROC curve was applied to detect the value of miR-506 in diagnosing CML and predicting the 5-year survival of patients, and K562 cell line was transfected with miR-506 inhibitor and miR-506 mimic for observing its effects on the cell proliferation and apoptosis. RESULTS: miR-506 in CML patients was evidently lower than that in healthy people, the AUC of diagnosis of miR-506 was 0.883, the total survival of patients with low miR-506 was evidently lower than those with high miR-506, and the AUC of predicted survival of patients was 0.778. The proliferation of cells transfected with miR-506 inhibitor was promoted, the apoptosis and the survival rate reduced. CONCLUSION: miR-506 is evidently reduced in CML, and may be applied as a diagnostic and predictive treatment for CML and 5-year related survival; it can also can hinder the viability of K562 cells and promote apoptosis.

The small-animal radiation research platform (SARRP): dosimetry of a focused lens system.

A small animal radiation platform equipped with on-board cone-beam CT and conformal irradiation capabilities is being constructed for translational research. To achieve highly localized dose delivery, an x-ray lens is used to focus the broad beam from a 225 kVp x-ray tube down to a beam with a full width half maximum (FWHM) of approximately 1.5 mm in the energy range 40-80 keV. Here, we report on the dosimetric characteristics of the focused beam from the x-ray lens subsystem for high-resolution dose delivery. Using the metric of the average dose within a 1.5 mm diameter area, the dose rates at a source-to-surface distance (SSD) of 34 cm are 259 and 172 cGy min(-1) at 6 mm and 2 cm depths, respectively, with an estimated uncertainty of +/-5%. The per cent depth dose is approximately 56% at 2 cm depth for a beam at 34 cm SSD.

Role and mechanism of decitabine combined with tyrosine kinase inhibitors in advanced chronic myeloid leukemia cells.

Patients with advanced chronic myeloid leukemia (CML) have a poor prognosis, with the use of tyrosine kinase inhibitors (TKIs) to treat CML demonstrating poor results. The results of the present study revealed that, following Cell Counting Kit-8 analysis, treatment of K562 cells with decitabine (DAC) combined with TKIs exhibits synergic effects. Co-immunoprecipitation indicated that tyrosine-protein phosphatase non-receptor type 6 (SHP-1) and BCR-ABL fusion protein (BCR-ABL) (p210) form a complex in the K562 cell line, and in the primary cells derived from patients with CML. These results suggested that SHP-1 serves a role in regulating the tyrosine kinase activity of BCR-ABL (p210). In addition, SHP-1 expression increased, while BCR-ABL expression decreased in the group treated with DAC and TKIs combined group compared with the TKI monotherapy group. Treatment with imatinib (IM) demonstrated no effect on SHP-1 methylation in the K562 cell line; however, the methylation of SHP-1 was not determined in the combined IM and DAC therapy group. Treatment with DAC demonstrated the ability to activate the expression of silenced SHP-1 through demethylation, thus decreasing BCR-ABL tyrosine kinase activity, resulting in an improved therapeutic effect on CML.

[Effect of Bortezomib on Proliferation, Apoptosis and SHP-2 Gene Expression of Lymphoma Cells].

OBJECTIVE: To investigate the effects of Bortezomib on proliferation, apoptosis and SHP-2 gene expression of lymphoma Jurkat cells and Raji cells. METHODS: Methylthiazoly tetrazolium assay (MTT) was used to observe the proliferation of Jurkat cells and Raji cells treated with bortezomib in different doses. Cell apoptosis was detected by morphological examination and flow cytometry. The level of SHP-2 mRNA expression before and after the treatment with bortezomib was measured by RT-PCR. RESULTS: Bortezomib could inhibit the proliferation of Jurkat and Raji cells and induce their apoptosis with time-and dose-dependent manner. After treatment with 5-100 nmol/L bortezomib, the expression of SHP-2 in Jurkat cells and Raji cells was upregulated. CONCLUSION: Bortezomib can inhibit the proliferation and induc the apoptosis of Jurkat and Raji cells obviously, upregulate the expression of SHP-2 mRNA, suggesting that the SHP-2 may participate in regulation of bortezomib induced apoptosis of Jurkat cells and Raji cells.